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Global transcriptional profiling changes upon knockout of USP22 in human Non-small cell lung cancer cells

ABSTRACT: Global transcriptional profiling changes upon knockout of USP22 in human Non-small cell lung cancer cells

PROVIDER: PRJNA545343 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9157010.fastq.gz	Fastqsanger.gz
	SRR9157011.fastq.gz	Fastqsanger.gz
	SRR9157012.fastq.gz	Fastqsanger.gz
	SRR9157013.fastq.gz	Fastqsanger.gz
	SRR9157014.fastq.gz	Fastqsanger.gz

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Global transcriptional profiling changes upon knockout of USP22 in human Non-small cell lung cancer cells

Project description:The experiment was designed to display differential gene expression profiling changes in two human non-small cell lung cancer cells A549 and H1299 upon knockout of USP22 gene, by using RNAseq technology.

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Changes in Treg gene expression upon deletion of Usp22 and Usp21

Project description:Usp22 and Usp21 are important for Foxp3 stability. We used RNA sequencing to determine the broad changes upon Usp22 and Usp21 deletionWe then performed gene expression profiling analysis using data obtained from RNA-seq and compared to each other

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Investigating the role of USP22 in reprogramming

Project description:Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) by overexpressing OCT4, SOX2, KLF4 and MYC. Although this cell fate transition is a slow and inefficient process, inhibiting several epigenetic barriers has shown to facilitate it. A previously employed epigenetic focused CRISPR-Cas9-mediated knockout screen during reprogramming uncovered novel human somatic cell reprogramming barriers. Here, I showed that USP22, target for gRNAs that were enriched in iPSCs from the screen, is a barrier for reprogramming and its loss is compatible with iPSC generation. Overexpressing wild-type or deubiquitinase mutant (C185A) USP22 in knockout background could rescue the phenotype. Additionally, knocking out other SAGA deubiquitinase subunits, ENY2 and ATXN7L3 did not increase the reprogramming efficiency. Mechanistically, we showed that USP22 loss upregulates an important pluripotency-related transcription factor, SOX2, expression even as early as 3 days after OSKM expression. We hypothesized that USP22 downregulates pluripotency-related gene expression during reprogramming independent from its SAGA integration and deubiquitinase activity. To address this, I will repeat rescuing USP22 knockout phenotype in reprogramming by overexpressing mutant versions of USP22 including K129R (acetyl inhibited) and HHAA (deubiqutinase). Additionally, I will check the expression of pluripotency-related genes at early time points of reprogramming upon USP22 knockout by transcriptome profiling. Lastly, I will generate USP22 knockout iPSC lines to force them to differentiation to observe if they have any problem with pluripotency exit. This work will establish a mechanistic understanding for the role USP22 play on both human somatic cell reprogramming, pluripotency and differentiation.

2023-07-31 | GSE225151 | GEO

An in vivo screening platform using PDX models reveals KEAP1, USP22 and other drivers of chemoresistance in small cell lung cancer

Project description:Small cell lung cancer (SCLC) is characterized by exquisite chemosensitivity followed by rapid emergence of chemoresistance. To identify genetic events that drive resistance to cisplatin-etoposide chemotherapy, we conducted cDNA overexpression and CRISPR knockout screens in an in vivo platform centered on chemosensitive patient derived xenograft (PDX) models of SCLC. cDNA overexpression screens revealed MYC, MYCN and MYCL as drivers of tumor cell growth through chemotherapy. CRISPR knockout screens identified the KEAP1/NRF2 pathway and members of the SAGA (Spt-Ada-Gcn5 acetyltransferase) complex, including the deubiquitylase USP22. We demonstrated that knockout of either KEAP1 or USP22 switches chemosensitive PDX models to become chemoresistant, with our data supporting distinct molecular consequences of each, including suppression of DNA damage signaling upon USP22 deletion. Data from the IMpower133 clinical trial revealed that a substantial proportion of SCLC patients exhibit KEAP1/NFE2L2 genetic alterations, with activation of an NRF2 transcriptional signature associated with reduced SCLC patient survival with chemotherapy.

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mRNA-seq of HCT116 USP22 knockdown cells

Project description:This analysis identifies genes which are affected in HCT116 cells upon USP22 knockdown

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mRNA-seq of SW480 USP22 knockdown cells

Project description:This analysis identifies genes which are affected in SW480 cells upon siRNA-mediated USP22 knockdown

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mRNA-seq of SW837 USP22 knockdown cells

Project description:This analysis identifies genes which are affected in SW837 cells upon siRNA-mediated USP22 knockdown

2019-12-06 | E-MTAB-8215 | biostudies-arrayexpress

mRNA-seq of MCF10A USP22 knockdown cells

Project description:This analysis identifies genes which are affected in MCF10A cells upon siRNA-mediated USP22 knockdown

2019-12-06 | E-MTAB-8247 | biostudies-arrayexpress

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Project description:RNA-seq analysis of sorted Usp22-WT and Usp22-KO tumor cells from subcutaneously implanted mouse pancreatic tumors

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Project description:USP22 plays oncogenic role and in order to study molecular mechanism of USP22 to promote tumorigenesis, microarray analysis was performed on USP22 knockdowned cells.

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